DUSP14 Antibody (C-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | O95147 |
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Clone Names | 4021108 |
Gene ID | 11072 |
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Other Names | Dual specificity protein phosphatase 14, MKP-1-like protein tyrosine phosphatase, MKP-L, Mitogen-activated protein kinase phosphatase 6, MAP kinase phosphatase 6, MKP-6, DUSP14, MKP6 |
Target/Specificity | The synthetic peptide sequence used to generate the antibody AP8456b was selected from the C-term region of human DUSP14. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | DUSP14 |
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Synonyms | MKP6 |
Function | Involved in the inactivation of MAP kinases. Dephosphorylates ERK, JNK and p38 MAP-kinases. Plays a negative role in TCR signaling by dephosphorylating MAP3K7 adapter TAB1 leading to its inactivation (PubMed:24403530). |
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Provided below are standard protocols that you may find useful for product applications.
Background
DUSP14 is involved in the inactivation of MAP kinases. This proein dephosphorylates ERK, JNK and p38 MAP-kinases. In addition to antigen recognition by the T-cell receptor, T-cell activation requires a second signal from a costimulatory receptor, such as CD28, which interacts with B7-1 (CD80) and B7-2 (CD86) ligands on antigen-presenting cells. CD28 costimulation induces transcription of interleukin-2 and stabilizes newly synthesized IL2 through the activation of mitogen-activated protein kinases (MAPKs), such as ERK and JNK, and the subsequent creation of AP1 transcription factor. DUSP14 is a negative regulator of CD28 signaling.
References
Marti, F., et al., J. Immunol. 166(1):197-206 (2001).
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